chemical hazards in the artisanal gold sector€¦ · elemental mercury, a silver liquid (fig. 1),...
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Mercury
Chemical hazards
in the artisanal gold sector
Impacts of mercury, cyanide and silica dust
on human health and environment
@ 2020 Artisanal Gold Council. All rights reserved.
Understanding occupational health risks
in the artisanal gold sector is an
important prerequisite for miners to
protect themselves and their communities,
and to transition to environmentally
sound and safe practices.
1
Chemical hazards
Mercury
Elemental mercury, a silver liquid (fig. 1), is a highly toxic heavy metal that cannot
be destroyed and persists in the environment. It is a deficient but simple and
cheap method to extract gold. Miners in artisanal gold mining are exposed to
elemental mercury during amalgamation (mixing ore with mercury), squeezing
(separating solid amalgam from excess mercury), vaporization (heating of
amalgam), smelting (melting sponge gold with residual mercury), and during
refining of raw gold doré.
Due to its high volatility, elemental mercury can
transform from its liquid state to vapour even at room temperature.
The vapour is odorless and colorless, but extremely toxic and very
adhesive. Therefore, inhaling elemental mercury vapours during ore
processing, and most intensively when burning amalgam, is the most
dangerous form of exposure. Lungs retain around 80% of the inhaled
vapours, from where the mercury enters the bloodstream.
Furthermore, mercury vapour can adsorb to clothes, skin, furniture,
work tools and walls. These materials can continue to emit high
concentrations of mercury for extended periods of time. Hence, the
whole household gets exposed to mercury vapours when mercury is
vaporized within the home or if work clothes and work equipment are
stored at home.
If liquid elemental mercury is accidentally ingested or comes into contact with unprotected skin, only
a very small amount gets absorbed by the body (less than 3%), but the exposure can cause skin and
eye irritation.
Occupational health risks in the artisanal gold sector
The Artisanal and Small-scale Gold Mining (ASGM) sector typically consists of small groups or
individuals extracting gold with semi-mechanized and low-tech methods. Mining sites tend to
have poor occupational safety standards and practices exposing miners to various occupational
health hazards. Chemical risks include the exposure to toxic substances such as mercury, cyanide
and silica dust. Other occupational health risks include painful disorders of the muscles and
skeleton (e.g. from heavy lifting), physical trauma (e.g., from slipping, falling, landslides) or
exposure to noise, heat and humidity. Furthermore, poor living conditions in artisanal mining
communities can increase the susceptibility to communicable diseases such as cholera, malaria
or tuberculosis.
This brochure provides a brief overview on the health and environmental impacts of mercury,
cyanide and silica dust in the sector. Chemical risks do not only affect miners, but also their
communities. Mercury and cyanide are both highly toxic to human health. However, only mercury
persists in the environment and can travel long distances in the environment. Exposure to very
fine silica dust is a common hazard in hard rock mining, but one that can easily be prevented.
Figure 1: Elemental
mercury (photo: AGC)
Figure 2: Elemental mercury is
mainly absorbed by the lungs
2
Mercury
Health data for artisanal gold mining communities is scarce and the prevalence and severity of
mercury intoxication differs depending on local practices. According to a global study, one in three
active miners and gold shop owners suffers from chronic elemental mercury vapour intoxication.
Mercury in the environment
The ASGM sector is responsible for around 38% of the global mercury emissions to the atmosphere
originating from human activity. Mercury in the atmosphere can travel over long distances. For
example, an estimated 95% of anthropogenic mercury deposited in Canada comes from sources
outside Canada, mainly East Asia. Elemental mercury is not only emitted to the atmosphere during
ore processing or from tailings, it is often also directly released into water streams and soils (e.g.,
from poorly made tailings ponds). Most of the mercury released into the environment will eventually
enter aquatic systems (streams, lakes, rivers and oceans) where bacteria can transform it into
methylmercury, the most toxic form of mercury (fig. 3, step 2&3). The transformation rate of
elemental mercury into methylmercury depends on many different physical, chemical, and biological
factors such as presence of specific bacteria, temperature and water flow. Therefore, it is difficult to
Figure 3: Impacts of mercury use in ASGM on human health and the environment: Mercury persists and travels in the
environment, affecting not only miners and their communities locally but also the global environment
3
Mercury
predict how much and how fast elemental mercury will be transformed into the more toxic and
bioavailable form of methylmercury. Once methylated, the toxins are absorbed by plankton and
methylmercury is concentrated up the food chain from plankton to shellfish (e.g., mussel, shrimp,
crab), to small fish, to larger predatory fish (e.g., bass, tuna, shark) and mammals (e.g., otters, whales).
Health effects of mercury exposure
Mercury intoxication can appear in three forms: as (1) acute or (2) chronic elemental mercury vapour
intoxication in artisanal gold mining, or (3) as chronic methylmercury intoxication.
(1) Acute elemental mercury intoxication in artisanal gold mining
A miner or bystander can suffer
from acute elemental mercury
intoxication, if the person inhales
very high concentrations of
elemental mercury vapours
during a vaporization event,
causing damage primarily to the
lungs and the digestive system.
Most symptoms usually develop
within a few hours after exposure,
starting often with
gastrointestinal symptoms
(nausea, vomiting). The vapours
can irritate the lips and mouth
(stomatitis), the gums (gingivitis)
as well as the respiratory tract,
causing a burning sensation in
the lungs (sore throat), a
tightness in the chest, shortness
of breath (dyspnea) and coughing.
Mercury vapours can also cause an inflammation of lung tissue (chemical pneumonitis) or edema
(swelling caused by excess fluid) with a potentially fatal collapse of the lungs. Additional symptoms
reported include excessive salivation, fever, chills, headache, weakness, high protein levels in urine
(proteinuria), high blood pressure (hypertension), irritation of eyes (uveitis) and skin as well as
vomiting and diarrhea that can lead to shock due to dehydration. Damage to the kidneys that can
lead to fatal kidney failure has also been reported.
In survivors, the acute mercury induced lung damage usually resolves completely, but long-term
problems such as lung restrictions have been reported. The absorbed mercury can cross the blood-
brain barrier which is a highly selective semipermeable border of cells that prevents solutes in the
blood from entering the nervous system. Mercury can enter the nervous system and cause
symptoms of chronic intoxication (e.g. neurological effects) several days after the initial exposure.
Figure 4: Major health impacts of mercury intoxication
4
Mercury
(2) Moderate & severe chronic elemental mercury intoxication
This form is most prevalent in artisanal mining communities and is caused if a miner or bystander is
regularly exposed to elemental mercury vapours over an extended length of time. Mercury
accumulates in the body and can cause moderate to severe symptoms of chronic elemental mercury
intoxication over time (fig. 4). Chronic intoxication mainly affects the brain and the kidneys.
Neurological symptoms include tremors in several parts of the body, lack of coordination and
movement control, memory impairment, shyness, sleep disorders, blurred vision and sensory
disturbances. Damages to kidneys such as proteinuria is more difficult to observe; it can become
apparent in symptoms such as swollen hands or feet and blood in the urine. In addition, irritation of
the mouth or the gums, loss of appetite and salivation, fatigue and weakened immune systems have
also been reported. People with moderate levels of intoxication usually have moderate pain levels
and can perform regular activities. However, people with severe intoxication are not able to perform
regular activities (e.g., buttoning a shirt because of tremors) and can have severe problems in
cognitive functions (e.g. paying attention or memorizing things).
Though some of the symptoms described can occur immediately after the exposure or a few days
later, chronic elemental mercury intoxication usually has a slow onset, with symptoms presenting up
to 5 to 10 years later. Some organ damage can be wholly or partially reversible, if further exposure
to mercury stops. The body excretes elemental mercury mainly through the urine and it takes around
60 to 90 days for the mercury body burden to fall to half (half-life). The risk of permanent organ
damage increases with the length and magnitude of elemental mercury exposure.
(3) Health impacts of chronic methylmercury intoxication through fish consumption
When a person consumes contaminated fish or shellfish (> 0.5 mcg MeHg/g fish) on a regular basis
over an extended period, methylmercury accumulates in the body and can cause chronic
methylmercury intoxication. The uptake and effects of methylmercury in the body are influenced by
several factors such as the exposure (frequency and dose of contaminated fish consumption), age
(higher vulnerability of fetuses, infants and children) or genetics (causing different sensitivities to
methylmercury). In addition, nutritional deficiencies (e.g., iron or folate) or alcohol consumption can
increase the uptake, whereas some foods (e.g., omega-3 fatty acids, vitamin E, garlic) seem to
attenuate the impact.
Frequent consumption of moderately to highly contaminated fish or shellfish causes methylmercury
to accumulate in the brain, causing similar neurological symptoms as chronic elemental mercury
exposure (tremors, lack of muscle coordination, behavioral, emotional and memory effects) (fig. 4).
Methylmercury also affects the cardiovascular system and can cause high blood pressure, heart
attack or coronary artery diseases. Other symptoms include headache, fatigue and reduced fertility
in men and women.
It is unclear whether exposure to low doses of methylmercury is toxic in adults. Several countries
and international organizations have issued guidelines on fish consumption to advise the general
population about safe fish-eating practices. Swordfish, for example, has one of the highest average
5
Mercury
concentrations of methylmercury (1 mcg/g fish), whereas tilapia is usually safe to consume (average
0.01 mcg/g fish). According to the Provisional Tolerable Weekly Intake (PTWI) of 1.6 mcg of mercury
per kg of body weight, a person weighing 50 kg can safely consume up to 80 grams of swordfish or
8 kg of tilapia per week. This example shows how the contamination of fish depends on the species.
Contamination levels of the same species, however, also vary between geographic catchment areas.
The provision of public information on which fish to eat and how often in a geographic region is
crucial.
Impact of mercury on developing fetuses, infants and children
Elemental and methylmercury have much higher detrimental effects
on fetuses, infants, and small children than on adults because their
central organs are still developing. Mercury can cross the placental
barrier in the mother’s womb. Because mercury accumulates in the
body, exposure of women even before the beginning of the
pregnancy can have negative impacts on the child.
Negative health outcomes from prenatal exposure to mercury
depend on the exposure level and can range from high blood
pressure, memory problems and deficits in fine motor skills to
impaired movement and coordination problems (cerebral palsy),
convulsions (seizures), severe intellectual disability, distortion of
limbs, and death. Effects of prenatal exposure to mercury may also
appear later on during child development, for example in the form
of learning disabilities during school age. Most of the damage
caused by mercury during prenatal exposure is permanent.
The effects of mercury on infants and children are less known. Since children have less body mass
and a proportionally higher lung volume, exposure to elemental mercury vapours or contaminated
fish leads to a higher body burden compared to adults. If present during amalgamation (fig. 5),
children can also be exposed to higher levels of mercury since they are closer to the ground and
therefore often closer to flames and vapours, compared to adults. Children are also at a higher risk
of playing with mercury or mercury contaminated items and can accidentally ingest or inhale it.
Lastly, mercury can also be transferred from the mother to the child via breastfeeding. However,
breast milk is important for the child’s development and mothers should not be discouraged from
breastfeeding.
The risk of permanent organ damage increases the earlier and the more infants and children are
exposed to mercury. Furthermore, acrodynia (‘pink disease’) has been reported among small
children. Acrodynia is characterized by body rash, swelling of extremities (edema), irritation of palms
and soles, skin peeling (desquamation) of hands and feet, abnormal dermal sensation such as
prickling (paresthesia), irritability, pain or discomfort due to the exposure of eyes to sunlight
(photophobia), fever, insomnia and profuse sweating.
Figure 5: A child gets exposed to
elemental mercury vapours during
vaporization (photo: AGC)
6
Mercury
Treatment of mercury intoxication
The medical treatment options for the different forms of mercury intoxication are limited. The most
important intervention is to stop any further mercury exposure at the mining site and/or through
the consumption of high-risk fish. If required, supportive care can alleviate symptoms, for example
the provision of supplemental oxygen for respiratory distress or physiotherapy for muscle control
problems. In addition, clinical tests might be necessary to assess any organ damage (e.g. renal
function test, electrocardiography (ECG)) and necessary treatments.
Chelation therapy is only advised to treat severe cases of acute elemental mercury intoxication.
Chelating agents bind to mercury in the bloodstream and remove it from the body through the
kidneys in the urine. However, the use of chelation therapy is controversial, and it is not advised for
chronic intoxication with elemental mercury or methylmercury. Once mercury has accumulated in
the organs, especially the brain, it is usually resistant to treatment with chelating agents.
Prevention at mining sites
Several interventions at work sites can protect miners and surrounding communities from mercury
exposure or at least reduce the risks for human health and environmental contamination (fig. 6).
These interventions reach from exposure prevention of most vulnerable groups (women at
childbearing ages, infants and children), to exposure reduction, to eventually the elimination of
mercury use through mercury free processing systems.
Figure 6: Risk pyramid of mercury use in artisanal gold mining
7
Cyanide
Cyanide
Cyanide is a rapidly acting, potentially deadly chemical that can exist in various forms: a colorless
gas (hydrogen cyanide), a colorless liquid, or in form of crystals, powder or pellets (cyanide salts such
as sodium cyanide). Cyanide is sometimes described as having a bitter almond smell, but it does not
always give an odor, nor can everybody detect it. Cyanide is a naturally occurring chemical
compound and is found in several plants (e.g. cassava roots, almonds) and in cigarette smoke.
Cyanide exposure in artisanal gold mining
Cyanide is used for gold extraction in many large-scale mining operations worldwide. In artisanal
mining, cyanide leaching techniques have been used in Asia and Latin America for several decades
and have more recently begun in Sub-Saharan Africa. With a gold recovery rate of around 60 to
90%, its performance is superior to mercury with a recovery rate of 20 to 50%, depending on the
processing system. Sometimes, cyanide is used to capture residual gold by leaching ore and tailings
to which mercury has previously been added – i.e. mercury contaminated materials. This is a worst
practice under the Minamata Convention since cyanide increases the environmental mobility of
mercury.
If cyanide is adequately handled, risks for human health and the environment can be minimized.
However, lack of safety precautions and inadequate tailings management are common in artisanal
gold mining and can cause negative impacts on miners, their communities and local aquatic systems.
Human health hazards include the inhalation of hydrogen cyanide gas, especially when the pH of
the cyanide solution is not maintained. This is most dangerous in enclosed, non-ventilated spaces.
Miners may also encounter skin contact if they are handling cyanide without protective gear, for
example when working with bare feet in cyanidation ponds (fig. 11, page 14). Furthermore, mining
communities can be exposed to contaminated water and food. Children can accidentally play with
containers containing cyanide pellets or crystals and poison themselves or can be exposed during
the cyanidation process. While the lungs and the gastrointestinal system can absorb high amounts
of cyanide, the absorption level through skin exposure is moderate (fig. 7).
If cyanide enters water bodies, fish and other aquatic biota are particularly sensitive to cyanide
exposure, causing death even at low concentrations.
Effects of cyanide on health
Cyanide is highly toxic. A small dose of ingested cyanide salts may be deadly within a short time
unless the person receives antidote therapy immediately after exposure. The inhalation of 120 to
150 mg/m3 can cause life-threatening injuries and may lead to death after 30 to 60 minutes;
exposure to over 300 mg/m3 is immediately fatal.
8
Cyanide
Similar to mercury, individual
factors such as age, nutritional
status or pre-existing medical
conditions impact cyanide
absorption rate. For example,
absorption is higher in people
with impaired renal function
(e.g., caused by chronic
mercury intoxication).
Once absorbed by the lungs,
the stomach or the skin,
cyanide is quickly distributed
through the body via the
blood stream. It prevents the
cells from absorbing oxygen,
causing cell death. Since the
heart and the brain use a lot of
oxygen, the impacts on these
organs are the most severe
(fig. 7). The symptoms vary
depending on the dose and frequency of exposure.
Low acute exposure: Symptoms of low, acute exposure include dizziness, headache, nausea and
vomiting, rapid breathing, rapid heart rate, restlessness, weakness, hypoxia (decrease of oxygen
supply to the brain) and skin and eye irritation. At low levels of exposure, most cyanide leaves the
body within 24 hours after exposure without any long-term health implications.
High acute exposure: In cases of high acute exposure, the following symptoms can occur in
addition to the low exposure effects described above: Convulsions (seizures), loss of consciousness,
low blood pressure, lung injury to the point of respiratory failure or coma (both fatal). Death can
occur within minutes and up to an hour after a lethal dose of cyanide gas and within minutes after
ingesting a lethal dose of cyanide salt.
Low chronic exposure: The effects of regular cyanide exposure over a longer period are poorly
understood. Yet, cyanide can damage the central nervous system (causing e.g., headaches, dizziness,
numbness, tremors, loss of visual acuity), the cardiovascular system (e.g., rapid heart rate) and the
respiratory system (e.g., breathing difficulties, chest pain). Furthermore, goiter (enlargement of the
thyroid gland) has also been observed. In a study among artisanal gold miners in Burkina Faso,
vomiting, abdominal pain, anxiety, changes in taste and bizarre behavior were reported in addition
to chest pain and headaches.
Children exposed to cyanide show similar symptoms as adults. However, smaller amounts of cyanide
are more harmful and can be fatal due to the lower body mass. Since cyanide can pass the placental
barrier of pregnant mothers, it also impacts the developing fetus. Children have been born with
thyroid disease due to prenatal exposure to cyanide.
Figure 7: Major health impacts of cyanide
9
Cyanide
Treatment of cyanide intoxication
Acute cyanide intoxication can be treated with antidotes and supportive medical care (esp. for
respiratory and cardiovascular symptoms). Antidotes are more effective if given immediately after
exposure, therefore seeking immediate medical care is important. If cyanide is ingested, activated
carbon can help to adsorb it in the gut and prevent the uptake in the blood stream. The carbon
should be used within the first hour after exposure; a single dose of 50g of activated charcoal in
adults and 1 g/kg, up to a maximum of 50g, in children. Since adequate medical care is often not
available in remote artisanal mining sites, risk mitigation becomes even more important. All
operations using cyanide should have an approved cyanide antidote kit on hand and a trained
person to administer the kit (in most cases intravenously) to the patient.
Cyanide in the environment
Cyanide is a serious risk to the environment when it contaminates soil and water, particularly to
aquatic life. For example, a free cyanide concentration of 20 mcg/L (about one small drop of cyanide
per liter) is fatal to fish. Therefore, safe handling of cyanide and adequate tailings management is
crucial!
Cyanide does not accumulate in plant life or animals over time like mercury, and it can be safely
used and destroyed if handled professionally. Unlike mercury, cyanide is a degradable chemical
compound which can be destroyed, either through cyanide removal (AVR process: acidification–
volatilization–reneutralization) or through natural oxidation to less toxic cyanide species. The natural
degradation process reduces the toxicity of cyanide species over time through different mechanisms
(fig. 8), mainly volatilization from surface water to hydrogen cyanide gas (concentrations in air are
usually low and not harmful to humans), atmospheric oxidation, absorption by other minerals,
photo-degradation
(destruction through sunlight)
and biodegradation
(biological oxidation) through
microorganisms such as
bacteria and plants. Cyanide
ultimately degrades into
nontoxic carbon dioxide and
nitrates.
In soil, cyanide can evaporate,
be transformed by
microorganisms or it can seep
into ground water where it is
less likely to be degraded due
to lack of sunlight and oxygen.
It has been detected in
groundwaters in contaminated Figure 8: Natural degradation processes of cyanide in tailings ponds
10
Cyanide
settings such as landfill leachates where it can sterilize microorganisms within the soil, consequently
preventing its degradation, causing the contaminated plume of groundwater to spread further.
The natural degradation rate for different cyanide species differs, depending on the factors
influencing the degradation processes, e.g., temperature, pH, intensity of light, surface area to depth
ratio of water bodies, solution agitation, and type of soil. Accordingly, the natural detoxification
process tends to be faster in tropical and subtropical climates where temperatures and light intensity
are higher. However, natural destruction rates are difficult to predict, and proper use of cyanide
requires effluent testing to ensure discharged waters are not toxic to fish. There is currently very little
formal data on the extent and environmental impact of cyanide use in artisanal gold mining, but
field observations show that its use is widespread and growing, and its environmental management
remains very poor to non-existent.
An additional management and environmental problem in artisanal gold mining is the use of cyanide
to leach mercury-contaminated tailings to capture residual gold. This is highly problematic because
cyanide dissolves not only gold but also mercury. This increases environmental mobility of mercury,
causing it to be more readily emitted to the atmosphere and increasing its bioavailability. Therefore,
this practice is considered a worst practice under the Minamata Convention. Unlike for mercury,
there is currently no international regulatory framework for cyanide use in artisanal mining. The
International Cyanide Management Code (ICMC) is a voluntary initiative of large-scale gold and
silver mining industries to standardize safe practices.
Preventive measures at artisanal mining sites
Health and environmental risks associated with cyanide use can be controlled through various
preventive measures:
Sodium cyanide decomposes on contact with acids, water and carbon dioxide, producing highly
toxic, flammable hydrogen cyanide gas; therefore, it should be stored in a dry, secure and well-
ventilated area in a closed container with a label signaling dangerous contents.
Workers should be alerted when cyanide is present and in use; smoking, eating and drinking should
not be allowed during this time. When handling cyanide, workers should wear personal protective
equipment (gloves, rubber boots, goggles, respirator); for example, wearing gloves while preparing
leach solutions to avoid skin contact.
pH is key! - One important safety aspect during ore processing with cyanide is the elevation of the
pH level through the addition of a base (calcium oxide (CaO) or lime). If the pH is not elevated to
above 10, toxic hydrogen cyanide gas forms and volatilizes. Mixing of solutions should also be
conducted in a ventilated area, in case there is a pH shock and hydrogen cyanide is off gassed.
Tailings containing cyanide should be managed to enhance the natural destruction of cyanide and
reduce environmental contamination. All effluents should be regularly tested; a fish test where live
fish is placed into the effluent outlet is a simple and an effective testing approach.
11
Silicosis
Silicosis
Silicosis is one of the most prevalent occupational diseases in the world, affecting millions of workers
in dusty industries such as mining, agriculture and construction. Silicosis is the most common form
of pneumoconiosis, the general term for dust borne interstitial lung diseases (examples of other
forms of dust are coal, cotton or asbestos). Crystalline silica minerals such as quartz and chalcedony
are basic components of soils, sands, and rocks like granites. Silica minerals form small particles
within dust.
Silica exposure in artisanal gold mining
The prolonged inhalation of dust during drilling,
mineral extraction, ore crushing and milling in the
mining sector causes fine silica to be deposited in
lungs. These deposits cause irritation of the lungs
(pneumonitis) and development of scar tissues (lesions,
nodules and fibroids), which in turn cause obstruction
of the airways (fig. 9). Silica particles can penetrate
different parts of the lungs depending on their size;
smaller particles are therefore most dangerous
because they can travel deeper into the respiratory
system and cause greater damage than larger
particles.
The exposure to silica usually goes unnoticed because
its inhalation does not cause any immediate health
effects such as lung irritation. Therefore, silicosis – one
of the oldest occupational diseases – is still considered
a hidden epidemic in many countries.
There are no international guidelines on occupational exposure limits to silica dust and national
occupational exposure thresholds vary between 0.025 and 3 mg/m3. The US National Institute for
Occupational Safety and Health (NIOSH) recommends an exposure limit (REL) of 0.05 mg/m3 as a
time-weighted average (TWA) for up to 10 hours/day during a 40-hour workweek. Some studies
have shown that this level does not provide sufficient protection and that only zero exposure can be
considered safe. According to OSHA (2016), the exposure to 0.05 mg/m3 over a period of 45 years
causes silicosis in 5 out of 100 people, the exposure to twice as much silica dust (to 0.1 mg/m3)
increases the risk to 30 in 100 people. Data on silica exposure in the artisanal mining sector are very
limited but field observations suggests it is extensive, especially in hard rock mining. A study in
Tanzania found average concentrations of 0.19 mg/m3 in aboveground operations, exceeding the
REL by four times. There are no reported data for below ground concentrations. Wet alluvial
processing usually poses a much lower exposure to silica dust compared to dry hard rock processing
and dry alluvial processing.
Figure 9: Inflammation and lung obstruction
caused by silica dust (© The State of Queensland)
12
Silicosis
Types of silicosis and symptoms
Miners can develop three different forms of silicosis, depending on the level of silica concentration
they are exposed to and the duration:
(1) Chronic silicosis (most common form) usually occurs after long-term exposure (over 10 to 20
years) to low concentrations of silica dust; the disease shows a slow progression.
(2) Accelerated silicosis occurs after exposure to larger amounts of silica over a shorter period of
time (5-15 years). The onset of symptoms is faster and evident between 5 to 10 years after
exposure.
(3) Acute silicosis (rare, unusual reaction) occurs after short-term and very intense exposure to high
amounts of silica that causes severe lung inflammation; it appears few weeks to months after
very intense exposure.
Common respiratory symptoms of silicosis are shortness of breath, cough and phlegm production.
An acute form of silicosis can also be accompanied by fever and chest pain. The severity of symptoms
depends on the dose and duration of exposure and individual factors such as smoking habits and
history of lung diseases that have weakened the lungs. This increases a person’s susceptibility to
silicosis. Genetic factors may also affect the clearance and defense mechanisms of the lungs.
Silicosis is irreversible and progressive (worsening with time), incurable and potentially fatal; it can
substantially shorten the life span of an affected miner. Since the onset of symptoms is usually slow
(several years), silicosis remains often undetected and undiagnosed. Furthermore, silicosis weakens
the respiratory system and increases the risk of comorbidities.
Tuberculosis, a communicable, opportunistic disease called silicotuberculosis in silicosis patients, is
a common comorbidity. Other health problems include lung cancer, chronic bronchitis (arising from
irritation of tubes that carry air to the lungs) and chronic obstructive lung disease (COPD). It is also
suspected to increase the risk of autoimmune diseases (body’s natural defense system fails to
differentiate its own cells from foreign cells, causing the body to mistakenly attack normal cells), e.g.
lupus erythematosus and rheumatoid arthritis.
Medical interventions
Silicosis cannot be treated or cured. It is only possible to ease symptoms for example through
supplemental oxygen or steroids to relax tubes, and cough medicine. If a person is diagnosed with
silicosis, the person should avoid any further exposure to silica dust and cigarette smoke. From a
public health perspective, the primary goal is therefore to detect workers exposed to silica as early
as possible through routine screening (e.g. regular occupational health check-ups with lung
functioning tests). Since artisanal mining sites often operate informally and/or without adequate
occupational and health protocols (e.g. no regular health check-ups at work site), medical
practitioners should ask patients working in the mining sector about any respiratory problems and
– if possible – test the lung functionality.
In order to prevent silicosis at the mining site, the two most important interventions are the use of
adequate respiratory masks and the use of water and wet processing techniques to suppress dust.
13
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cation/global-mercury-assessment-2018.
Veiga, M., Metcalf, S., Baker, R., et al. (2006).
Manual for Training Artisanal and Small-Scale
Gold Miners. UNIDO, Global Mercury Project.
Retrieved from http://archive.iwlearn.net/global
mercuryproject.org/documents/documents.htm.
Weinstein, M., & Bernstein, S. (2003). Pink ladies:
Mercury poisoning in twin girls. Cmaj, 168(2),
201.
WHO & UNEP (2008). Guidance for identifying
populations at risk from mercury exposure.
WHO, Geneva. Retrieved from
https://www.who.int/foodsafety/publications/ris
k-mercury-exposure/en/
Cyanide
ATDSR (2006). Public Health Statement Cyanide.
Retrieved from:
https://www.atsdr.cdc.gov/phs/phs.asp?id=70&t
id=19.
ATSDR (2006). Toxicological profile for Cyanide.
Agency for Toxic Substances and Disease
Registry, Georgia. Retrieved from
https://www.atsdr.cdc.gov/toxprofiles/tp.asp?id
=72&tid=19.
CDC (2018). Facts About Cyanide. Retrieved from:
https://emergency.cdc.gov/agent/cyanide/basic
s/facts.asp.
Graham J., & Traylor J. (2019). Cyanide Toxicity. In:
StatPearls. Treasure Island. Retrieved from:
https://www.ncbi.nlm.nih.gov/books/NBK50779
6/.
Figure 10: A miner preparing the mercury gold amalgam
for vaporization (photo: AGC)
14
References
Knoblauch, A., Farnham, A., Ouba, J., et al. (2020).
Potential health effects of cyanide use in
artisanal and small-scale golf mining in Burkina
Faso. Journal of Cleaner Production 252:
110689.
Marsden, J. & House, I. (2006). The Chemistry of
Gold Extraction. Society for Mining, Metallurgy,
and Exploration.
Veiga, M., Metcalf, S., Baker, R., Klein, B., Davis, G.,
Bamber, A., Siegel, S. & Singo, P. (2006). Manual
for Training Artisanal and Small-Scale Gold
Miners. UNIDO, Global Mercury Project.
Retrieved from
http://archive.iwlearn.net/globalmercuryproject.
org/documents/documents.htm.
Simeonova, F.P., Fishbein, L., World Health
Organization & International Programme on
Chemical Safety (2004). Hydrogen cyanide and
cyanides: human health aspects. World Health
Organization. Retrieved from:
https://apps.who.int/iris/handle/10665/42942.
Silicosis
Álvarez, R. F., González, C. M., et al. (2015).
Guidelines for the Diagnosis and Monitoring of
Silicosis. Archivos de Bronconeumologica 52 (2):
86-93.
CDC (2014): Preventing Silicosis and Deaths in
Construction Workers. Retrieved from:
https://www.cdc.gov/niosh/docs/96-
112/default.html.
Gottesfeld, P., Andrew, D., & Dalhoff, J. (2015).
Silica Exposures in Artisanal Small-Scale Gold
Mining in Tanzania and Implications for
Tuberculosis Prevention. Journal of
Occupational and Environmental Hygiene, 12(9).
Gottesfeld, P. (2018). International silica
standards: Countries must update exposure
limits. International Safety & Hygiene News.
Retrieved from:
https://www.ishn.com/articles/109495-
international-silica-standards-countries-must-
update-exposure-limits.
NIH (2020): Silicosis. Retrieved from:
https://medlineplus.gov/ency/article/000134.ht
m.
Pollard, K. M. (2016). Silica, silicosis, and
autoimmunity. Frontiers in Immunology, 7, 1–7.
Shafiei, M., Ghasemian, A., Eslami, M., et al. (2019).
Risk factors and control strategies for
silicotuberculosis as an occupational disease.
New Microbes and New Infections, 27, 75–77.
Sharma, N., Kundu, D., Dhaked, S., & Das, A.
(2016). Silicosis and silicotuberculosis in India.
Bulletin of the World Health Organization,
94(10), 777–778.
State of Queensland, Department of Natural
Resources, Mines & Energy (2020). What is
CWP? Retrieved from:
https://www.dnrme.qld.gov.au/miners-health-
matters/what-is-cwp.
Figure 11: A miner stands on a batch of ore in a heap
leaching pit, which uses cyanide as leaching agent
(Photo: AGC)
Figure 12: Dust exposure in artisanal hard rock mining is
a common threat (Photo: AGC)
AGC’s health program
Our Activities
Capacity development
o Gender-sensitive training for miners and
communities on occupational and safety
hazards in artisanal mining and community
health problems
o Capacity building for health care
professionals to detect, diagnose and treat
ASGM related health hazards including
mercury intoxication, and to provide
information on risk prevention
Research & monitoring
o Research on health hazards and their
relation to livelihoods in artisanal mining
communities
o Institutional capacity assessments of the
health care sector
o Developing strategies for creating national
health data infrastructure to monitor the
disease burden in ASGM communities and
evaluate health programs
Public health policies
o Policy consultation for governments to
develop Public Health Strategies for the
ASGM sector as part of the National Action
Plan to meet the goals of the Minamata
Convention on Mercury
Health as cross-cutting issue
o AGC considers health as cross-cutting issue
in all other interventions such as process
engineering, geology & geochemistry,
environmental management, and access to
finance and markets.
About the AGC
The Artisanal Gold Council (AGC) is a
not-for-profit organization dedicated to
improving the economic opportunities
and livelihoods of the millions of people
involved in the artisanal and small-scale
gold mining sector (ASGM) in 80+
countries.
Our integrated approach seeks to build
an environmentally sound, socially
responsible, and formalized ASGM
sector effective at transferring wealth
from rich to poor.
Contact us
Artisanal Gold Council
633 Courtney Street, Suite C#100
Victoria, BC Canada V8W 1B9
Tel. +1-250-590-9433
info@artisanalgold.org
artisanalgold.org
Our Publications
download from our website
@ 2020 Artisanal Gold Council. All rights reserved.
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